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Preservation of cerebral oxidative metabolism in fulminant hepatic failure: An autoregulation study

โœ Scribed by Larsen, Fin Stolze ;Ejlersen, Ellen ;Clemmesen, Jens Otto ;Kirkegaard, Preben ;Hansen, Bent Adel


Publisher
Wiley (John Wiley & Sons)
Year
1996
Tongue
English
Weight
480 KB
Volume
2
Category
Article
ISSN
1074-3022

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โœฆ Synopsis


Under normal conditions cerebral blood flow (CBF) is regulated to secure oxidative brain metabolism, but in patients with fulminant hepatic failure (FHF), insufficient CBF has been suggested to precede cerebral edema and intracranial hypertension. In order to determine if insufficient CBF and hypoxia are present in patients with FHF we increased the mean arterial pressure and measured cerebral metabolism. In six patients with FHF CBF determined by 133Xenon injection technique, transcranial Doppler mean flow velocity in the middle cerebral artery ( V , , , , ) and cerebral metabolism were determined, before and after an increase in mean arterial pressure by norepinephrine infusion. Mean arterial pressure was measured in a radial artery, and blood samples from the radial artery and internal jugular vein allowed calculation of the cerebral arteriovenous oxygen (AVD, , ), --glucose (AVDgI), and -lactate (AVD, , , ) differepatic encephalopathy and cerebral edema are H associated with a high mortality in patients with acute liver failure. It is poorly understood to what extent changes in cerebral circulation have pathophysiological significance, but recent studies have indicated that insufficient cerebral blood flow (CBF) could be of importance. 1,2 Normally, sufficient oxygen delivery for brain metabolism is secured by accurate regulation of CBF,3,4 but in patients with fulminant hepatic failure (FHF) and in rats with thioacetamide-induced liver failure, part of this regulation may be i m ~a i r e d . ~. ~ In case of circulatory instability with low systemic vascular resistance episodes of arterial hypotension From the Departments of *Hepatology, fAnestheria and the


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